The Gut-Brain Axis and Advancing Treatment for Depression
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The first link between depression and an unhealthy gut biome was stumbled across in 1980. Since then the pile of research has grown for decades, and today there is more evidence linking depression to gut inflammation than there is to “serotonin imbalance”. While many current anti-depressants absolutely work for some, they don’t work for everyone. Exploration into ketamine treatment and more emphasis on lifestyle changes has grown to find options for patients who anti-depressants aren’t as effective for. Today, we have a lot of research that shows the gut-brain axis can be a culprit leading to depression.
Research has shown that the “chemical imbalance” theory was disproven in the early 2000’s but the concept is kept alive because it helps prescribe anti-depressants that do work for many. Ketamine has recently been approved for the treatment of depression, and some have called it life-changing. However, it appears that ketamine is a positive experience for about 75% of patients and can either be ineffective or a terrifying trip for others. Animal studies and post-mortem studies show a higher percentage that those with severe depression had leaks in the blood-brain barrier. It’s thought that this permeability allows for damage or changes to neurotransmitters. Some studies show that when administering pro-inflammatory agents to people who don’t have depression, “had blunted responses in brain areas associated with reward, such as the ventral striatum. Inflammation also seems to decrease the release of dopamine, a neurotransmitter implicated in reward and movement.”
Despite the strong connections between the gut-brain axis and depression, it’s been challenging to treat depression with anti-inflammatory drugs. One of the biggest studies showed only 30% of participants improved when using an anti-inflammatory and some other big studies haven’t seen a change by prescribing anti-inflammatories. Lack of improvement with anti-inflammatories could be due to a couple of reasons. One is that the patient’s “flavor of depression” needs to be narrowed down; there can be different or overlapping factors causing depression. Another culprit could also be that an anti-inflammatory drug is a surface-level treatment that doesn’t change diet, exercise, sleep, and stress for a patient.
Expert Takeaways:Andrew Miller (a psychiatry professor at Emory):“We’ve come to the tipping point. And we know enough at this point to begin to target the immune system and its downstream effects on the brain to treat depression. We are there.”
Charles Raison, a professor of human psychology, human ecology and psychiatry at the University of Wisconsin at Madison:More clinical tests for inflammatory markers may be a way to differentiate the effectiveness
Keep Reading (10 min): Washington Post How Inflammation May Explain Depression